However, our finding of a predominantly low IL10 expression combined with high IFNG expression in the highly responsive cluster group B, might be consistent with a high Th1/Th2 balance, a known marker of an appropriate anti-tumor immune response [ 50].
Clearly, changes in α correspond to changes in the combined marker expression, and thus to transitions between complex regulatory network activation patterns.
In addition, our results showed that the combined marker expression levels correlated with tumor differentiation and tumor cell proliferation.
Multivariate analyses of the combined marker expression levels showed that patients with high expression level of all three markers had a shorter OS compared to patients with low expression of all the enzymes (p = 0.03, HR = 1.49, 95% CI = 1.07-2.08).
We found no evidence of statistical interaction between any of the assessed markers (data not shown) and, therefore, calculated predicted marginal survival probabilities for given marker expression patterns directly from the combined Poisson model including AZGP1, MUC1, and p53.
Based on this finding, Neumeister et al. set out to establish the significance of combined CSC marker expression by investigating the expression of CD44 and ALDH1A1 in a cohort of 639 primary breast tumours [ 17].
In this study, we investigated the changes in platelet activation, aggregation and cell surface marker expression in response to the combined exposure to advanced glycation end products and sidestream tobacco smoke extracts or nicotine.
The relationship between single-marker expression or combined-marker expression and established prognostic factors was investigated using the Pearson χ test.
Predicted marginal 5-year survival probabilities were calculated from the combined model for every combination of marker expression.
Combined, however, the CD marker expression profiles of the NP subtypes do support a mesenchymal origin of the immortal NP clones.
